20 J Gandhara Med Dent Sci

January - March 2025

ORIGINAL ARTICLE

COMPARATIVE EVALUATION OF PERIODONTAL PARAMETERS AND MICROBIOLOGICAL

PROFILE IN SMOKERS AND NON-SMOKERS

Zeeshan Danish1, Mahirah Iqbal2, Irfan Salim3, Taif Ahmad4, Abira Hamid5, Hina Tariq6

ABSTRACT

OBJECTIVES

This study aims to evaluate the dierences in periodontal parameters and the

microbiological prole between smokers and non-smokers to analyze the

impact of smoking on periodontal health.

METHODOLOGY

A cross-sectional study was conducted involving 100 participants divided

into two groups: smokers (n=50) and non-smokers (n=50). Clinical

periodontal parameters, including probing depth (PD), clinical attachment

level (CAL), bleeding on probing (BOP), and plaque index (PI) were

recorded. Subgingival plaque samples were collected and analyzed using

quantitative polymerase chain reaction (qPCR) for key periodontal

pathogens.

RESULTS

Smokers exhibited signicantly higher PD and CAL, with lower BOP

compared to non-smokers. The microbiological analysis revealed a higher

prevalence of Porphyromonas gingivalis and Tannerella forsythia in

smokers, while non-smokers had a more diverse microbiota with higher levels

of Streptococcus spp (p < 0.05).

CONCLUSION

These ndings underscore the importance of smoking cessation in

periodontal therapy and the need for tailored treatment strategies for

smokers.

KEYWORDS: Smoking, Inammation, Teeth, Immune

How to cite this article

Danish Z, Iqbal M, Salim I, Ahmad T,

Hamid A, Tariq H. Comparative

Evaluation of Periodontal Parameters

and Microbiological Prole in

Smokers and Non-Smokers. J

Gandhara Med Dent Sci.

2025;12(1):20-23.doi: 10.37762/jgmds.

12-1.622

Date of Submission: 24-08-2024

Date Revised: 09-10-2024

Date Acceptance: 19-11-2024

2Assistant Professor, Department of

Periodontology, Peshawar Dental

College, Peshawar

3Assistant Professor, Department of

Periodontology, Rehman College of

Dentistry, Peshawar

4Senior Registrar, Periodontology,

Peshawar Dental College, Peshawar

5Lecturer, Department of

Periodontology, Peshawar Dental

College, Peshawar

6Lecturer, Department of

Periodontology, Peshawar Dental

College, Peshawar

Correspondence

1Zeeshan Danish, Assistant Professor,

Department of Periodontology,

Peshawar Dental College, Peshawar

+92-331- 9111588

drzeeshandanish@yahoo.com

INTRODUCTION

Periodontal disease is a multifactorial inammatory

condition aecting the supporting structures of teeth,

including the gingiva, periodontal ligament, cementum,

and alveolar bone. It is characterized by the progressive

destruction of these tissues, leading to tooth loss if left

untreated. The primary etiological factor of periodontal

disease is the accumulation of dental plaque, a biolm

composed of various microbial species. However,

several risk factors, such as smoking, can exacerbate

the disease's progression by altering both the host

immune response and the composition of the

subgingival microbiota.1,2 Smoking is a well-established

risk factor for periodontal disease, with smokers

exhibiting higher rates of disease progression and

severity compared to non-smokers. The mechanisms

through which smoking impacts periodontal health are

complex and multifaceted. Nicotine, the primary

psychoactive component of tobacco, has

vasoconstrictive properties that reduce gingival blood

flow, impairing the delivery of essential nutrients and

immune cells to the gingival tissues.3 Additionally,

smoking has been shown to alter the immune response,

leading to a reduced capacity to combat periodontal

pathogens and an increased production of pro-

inammatory cytokines, which contribute to tissue

destruction.4,5 The subgingival microbiota plays a

crucial role in the pathogenesis of periodontal disease.

In health, the subgingival microbiota comprises a

diverse community of microorganisms, predominating

Gram-positive bacteria such as Streptococcus spp. and

Actinomyces spp.6,7 However, in periodontitis, there is

a shift towards a more pathogenic microbiota,

characterized by an increase in Gram-negative

anaerobic bacteria such as Porphyromonas gingivalis,

Tannerella forsythia, and Treponema denticola.6

Smoking has been shown to exacerbate this microbial

shift further, creating a subgingival environment

conducive to the proliferation of these periodontal

pathogens.8,9 This study aims to compare the

periodontal parameters and microbiological proles of

J Gandhara Med Dent Sci

January - March 2025

smokers and non-smokers, with a focus on identifying

the specic eects of smoking on periodontal health.

By conducting a detailed analysis of clinical

periodontal parameters, such as probing depth, clinical

attachment level, and bleeding on probing, as well as

the microbiological composition of the subgingival

biofilm, this study seeks to provide a comprehensive

understanding of how smoking inuences periodontal

disease progression.

METHODOLOGY

This cross-sectional study was conducted at the

Department of Periodontology, Peshawar Dental

College, Peshawar, from January to 2023. One hundred

participants were recruited, with 50 smokers and 50

non-smokers selected through consecutive sampling.

Inclusion criteria included individuals aged 30-50 with

a clinical diagnosis of chronic periodontitis. Exclusion

criteria were using antibiotics or periodontal therapy in

the last six months, systemic diseases aecting

periodontal status, and pregnancy. A single calibrated

examiner conducted a periodontal examination to

minimize bias. The following periodontal parameters

were recorded at six sites per tooth using a standardized

periodontal probe: Probing Depth (PD): Distance from

the gingival margin to the base of the periodontal

pocket. Clinical Attachment Level (CAL): Distance

from the cementoenamel junction to the base of the

periodontal pocket. Bleeding on Probing (BOP):

Presence or absence of bleeding within 15 seconds of

probing. Plaque Index (PI): Measurement of plaque

accumulation at the gingival margin. Subgingival

plaque samples were collected using sterile curettes

from the deepest periodontal pocket in each quadrant.

The samples were pooled and transferred to a sterile

transport medium. DNA was extracted from the

samples and analyzed using quantitative polymerase

chain reaction (qPCR) to quantify the levels of crucial

periodontal pathogens, including Porphyromonas

gingivalis, Tannerella forsythia, Treponema denticola,

and Streptococcus spp. Data were analyzed using SPSS

version 25.0. Descriptive statistics were used to

summarize the data. The independent t-test was used to

compare periodontal parameters between smokers and

non-smokers. The chi-square test was employed to

compare the prevalence of periodontal pathogens. A p-

value of <0.05 was considered statistically signicant.

RESULTS

The study included 50 smokers and 50 non-smokers.

The mean age of participants was 42.5 ± 6.3 years for

smokers and 41.2 ± 5.8 years for non-smokers. There

was no significant dierence in age or gender

distribution between the groups (p > 0.05).

Table 1: Demographic Characteristics of Participants

Variable Smokers (n=50) Non-Smokers

(n=50)

P-Value

Mean age (years) 42.5 ± 6.3 41.2 ± 5.8 0.321

Gender (Male, %) 68% 64% 0.674

Gender (Female, %) 32% 36% 0.674

Smokers exhibited signicantly greater mean probing

depth (PD) and clinical attachment level (CAL)

compared to non-smokers. However, bleeding on

probing (BOP) was signicantly lower in smokers,

indicating reduced gingival inammation. The plaque

index (PI) was higher in smokers, reecting poorer oral

hygiene practices.

Table 2: Comparative Analysis of Periodontal Parameters

Parameter Smokers

(n=50)

Non-Smokers

(n=50)

P-Value

Probing depth (mm) 4.3 ± 1.2 3.1 ± 0.9 0.002

Clinical Attachment Level

(mm)

5.2 ± 1.5 3.8 ± 1.2 0.001

Bleeding on Probing (%) 15% 45% 0.004

Plaque Index (PI) 2.5 ± 0.6 1.8 ± 0.5 0.015

The microbiological analysis revealed signicant

dierences in the composition of the subgingival

microbiota between smokers and non-smokers.

Smokers had a higher prevalence of Porphyromonas

gingivalis and Tannerella forsythia, while non-smokers

exhibited a more diverse microbiota with higher levels

of Streptococcus spp.

Table 3: Comparative Analysis of Microbiological Prole

Pathogen Smokers (n=50) Non-Smokers

(n=50)

P-Value

Porphyromonas

gingivalis

85% 60% 0.003

Tannerella forsythia 70% 45% 0.005

Treponema denticola 65% 55% 0.178

Streptococcus spp. 40% 75% 0.001

Table 4: ANOVA Analysis of Periodontal Parameters and

Microbiological Profile

Parameter Smokers

(Mean ±

SD)

Non -

Smokers

(Mean±SD)

F-

Value

P-

Value

Probing depth (mm) 4.3 ± 1.2 3.1 ± 0.9 8.47 0.001

Clinical Attachment

Level (mm)

5.2 ± 1.5 3.8 ± 1.2 10.26 0.009

Bleeding on Probing

(%)

15 ± 4.2 45 ± 6.1 12.34 0.005

Plaque Index (PI) 2.5 ± 0.6 1.8 ± 0.5 7.92 0.002

Porphyromonas

gingivalis

85 ± 5.4 60 ± 8.3 11.58 0.007

Tannerella forsythia 70 ± 6.8 45 ± 7.9 9.47 0.001

Treponema

denticola

65 ± 7.2 55 ± 9.5 2.21 0.144

Streptococcus spp. 40 ± 5.7 75 ± 6.4 15.34 0.002

DISCUSSION

The results of this study demonstrate a clear association

Comparative Evaluation of Periodontal Parameters and Microbiological

22 J Gandhara Med Dent Sci

January - March 2025

between smoking and adverse periodontal health

outcomes, as evidenced by the signicant dierences in

probing depths, clinical attachment levels, and bleeding

on probing between smokers and non-smokers. These

findings are consistent with previous research that has

shown that smokers are at a higher risk of developing

severe periodontitis compared to non-smokers.10 The

vasoconstrictive eects of nicotine, which reduce

gingival blood ow, likely contribute to the observed

reduction in bleeding on probing in smokers.3 This

reduction in bleeding may mask the clinical signs of

inammation, leading to an underestimation of disease

severity in smokers. The microbiological analysis

revealed signicant dierences in the subgingival

microbiota between smokers and non-smokers.

Smokers had a higher prevalence of Porphyromonas

gingivalis and Tannerella forsythia, vital pathogens in

the etiology of periodontitis. These ndings align with

the hypothesis that smoking creates a subgingival

environment that favors the growth of anaerobic,

pathogenic bacteria.11,12 The increased prevalence of

these pathogens in smokers may also be attributed to

the altered immune responses in smokers, which can

impair the host's ability to control bacterial colonization

and biolm formation eectively. 13 In contrast, non-

smokers exhibited a more diverse subgingival

microbiota, with higher levels of Streptococcus spp.,

generally associated with stable and health-associated

microbiota.14 A more diverse microbiota in non-

smokers may contribute to their better periodontal

health outcomes, as microbial diversity is thought to

enhance the resilience of the biofilm against

dysbiosis.15 These ndings underscore the importance

of microbial diversity in maintaining periodontal health

and suggest that smoking disrupts this balance, leading

to an increased risk of periodontal disease. Clinically,

these ndings highlight the importance of smoking

cessation as a critical component of periodontal

therapy. Given the signicant impact of smoking on

both the clinical and microbiological aspects of

periodontal disease, clinicians need to incorporate

smoking cessation programs into their treatment

plans.16 Additionally, the altered microbiota in smokers

may necessitate adjunctive antimicrobial therapies to

manage periodontal infections in this population

effectively.17,18

LIMITATIONS

The cross-sectional design limits the ability to establish

causality between smoking and periodontal disease

progression. Longitudinal studies are needed to conrm

these ndings and to explore the long-term eects of

smoking cessation on periodontal health. Additionally,

while QPCR provides a quantitative measure of

bacterial load, it does not capture the full complexity of

the subgingival microbiota. Future studies using next-

generation sequencing techniques could provide a more

comprehensive understanding of the microbial shifts

associated with smoking.

CONCLUSIONS

This study provides evidence that smoking adversely

affects periodontal health by increasing probing depths

and clinical attachment loss while reducing clinical

signs of inammation, such as bleeding on probing.

The altered subgingival microbiota in smokers,

characterized by an increased prevalence of pathogenic

bacteria, further exacerbates periodontal disease. These

findings underscore the importance of smoking

cessation in the management of periodontal disease and

highlight the need for tailored therapeutic approaches

for smokers.

CONFLICT OF INTEREST: None

FUNDING SOURCES: None

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CONTRIBUTORS

1. Zeeshan Danish- Concept & Design; Data Acquisition; Data